TY - JOUR
T1 - Renal and segmental artery hemodynamics during whole body passive heating and cooling recovery
AU - Chapman, Christopher L.
AU - Benati, Julia M.
AU - Johnson, Blair D.
AU - Vargas, Nicole T.
AU - Lema, Penelope C.
AU - Schlader, Zachary J.
N1 - Publisher Copyright:
© 2019 the American Physiological Society.
PY - 2019
Y1 - 2019
N2 - High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr; 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, n = 24 during thermal stress, n = 12 during CPTs) or the middle portion of a segmental artery (Segmental, n = 12). RVR was calculated as mean arterial pressure divided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: By 1.0 ± 1.0 mmHg•cm-1•s, Segmental: By 2.2 ± 1.2 mmHg•cm-1•s, P ± 0.03), and these increases were abolished with passive heating (P = 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline (P ± 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery. NEW & NOTEWORTHY Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.
AB - High environmental temperatures are associated with increased risk of acute kidney injury, which may be related to reductions in renal blood flow. The susceptibility of the kidneys may be increased because of heat stress-induced changes in renal vascular resistance (RVR) to sympathetic activation. We tested the hypotheses that, compared with normothermia, increases in RVR during the cold pressor test (CPT, a sympathoexcitatory maneuver) are attenuated during passive heating and exacerbated after cooling recovery. Twenty-four healthy adults (22 ± 2 yr; 12 women, 12 men) completed CPTs at normothermic baseline, after passive heating to a rise in core temperature of ~1.2°C, and after cooling recovery when core temperature returned to ~0.2°C above normothermic baseline. Blood velocity was measured by Doppler ultrasound in the distal segment of the right renal artery (Renal, n = 24 during thermal stress, n = 12 during CPTs) or the middle portion of a segmental artery (Segmental, n = 12). RVR was calculated as mean arterial pressure divided by renal or segmental blood velocity. RVR increased at the end of CPT during normothermic baseline in both arteries (Renal: By 1.0 ± 1.0 mmHg•cm-1•s, Segmental: By 2.2 ± 1.2 mmHg•cm-1•s, P ± 0.03), and these increases were abolished with passive heating (P = 0.76). At the end of cooling recovery, RVR in both arteries to the CPT was restored to that of normothermic baseline (P ± 0.17). These data show that increases in RVR to sympathetic activation during passive heating are attenuated and return to that of normothermic baseline after cooling recovery. NEW & NOTEWORTHY Our data indicate that increases in renal vascular resistance to the cold pressor test (i.e., sympathetic activation) are attenuated during passive heating, but at the end of cooling recovery this response returns to that of normothermic baseline. Importantly, hemodynamic responses were assessed in arteries going to (renal artery) and within (segmental artery) the kidney, which has not been previously examined in the same study during thermal and/or sympathetic stressors.
KW - Cold pressor test
KW - Doppler ultrasound
KW - Heat stress
KW - Renal blood velocity
KW - Renal vascular resistance
KW - Sympathetic activation
KW - Whole body cooling
UR - http://www.scopus.com/inward/record.url?scp=85073182687&partnerID=8YFLogxK
U2 - 10.1152/japplphysiol.00403.2019
DO - 10.1152/japplphysiol.00403.2019
M3 - Article
C2 - 31414950
AN - SCOPUS:85073182687
SN - 8750-7587
VL - 127
SP - 974
EP - 983
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 4
ER -